Transforming growth factor-β (TGF-β) is a key protein family member that includes activins, inhibins, and bone morphogenetic proteins (BMPs). It is essential in numerous biological processes, such as chemotaxis, apoptosis, differentiation, growth, and cell migration. TGF-β receptors initiate signaling through two primary pathways: the canonical pathway involving Smad proteins and non-canonical pathways that utilize alternative signaling mechanisms. When TGF-β signaling is disrupted, it has been shown to contribute to the development of various diseases, including cancer. Initially, TGF-β effectively inhibits the cell cycle and promotes apoptosis. However, its role can transition to facilitating tumor growth and metastasis as the disease progresses. Moreover, TGF-β drives cancer progression through epithelial–mesenchymal transition (EMT), modulation of factor expression, and evasion of immune responses. This complexity establishes the need for further research, particularly into pharmacological agents targeting TGF-β, which are emerging as promising therapeutic options. Current clinical and preclinical studies are making significant strides toward mitigating the adverse effects of TGF-β. This underscores the critical importance of understanding its underlying mechanisms to enhance treatment effectiveness and improve survival rates for cancer patients.

Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide and are driven by the interplay between oxidative stress and chronic inflammation. Although these processes have been extensively investigated, their integration into a unified mechanistic framework and their translational relevance for biomarker-guided precision medicine remain insufficiently addressed. This narrative review integrates mechanistic, biomarker, and translational perspectives on the redox–inflammation axis in atherosclerosis and acute ischemic stroke, critically evaluating oxidative and inflammatory biomarkers while highlighting current challenges and emerging therapeutic opportunities. Reactive oxygen and nitrogen species (ROS/RNS) promote endothelial dysfunction, lipid oxidation, and activation of redox-sensitive pathways, including NF-κB, Nrf2/Keap1, JAK/STAT, and the NLRP3 inflammasome, resulting in vascular inflammation and injury. Biomarkers such as hs-CRP, IL-6, MPO, MDA, F2-isoprostanes, oxLDL, and antioxidant enzyme activity have demonstrated associations with cardiovascular risk, disease severity, and clinical outcomes, and therefore show diagnostic and prognostic potential. However, with the exception of selected inflammatory biomarkers, most oxidative stress biomarkers have not yet been sufficiently validated for routine clinical use because of biological variability, limited specificity, and insufficient analytical standardization. Disappointing outcomes of antioxidant supplementation further reflect the complexity of redox biology and the dual physiological and pathological roles of ROS. Here, we highlight that future progress in cardiovascular medicine will require a shift from non-specific antioxidant supplementation to precision redox modulation, integrating multimarker profiling, system biology, multi-omics, and artificial intelligence and machine-learning approaches to improve cardiovascular risk stratification and personalized therapy.